Gene Report
Basic Info
Approved Symbol |
NCAM1
|
Symbol Alias |
NCAM, CD56 |
Approved Name |
neural cell adhesion molecule 1 |
Location |
11q23-q24 |
Position |
chr11:112831995-113149158, + |
External Links |
HGNC: 7656
Entrez Gene: 4684
Ensembl: ENSG00000149294
UCSC: uc001pnq.2
|
No. of Studies |
0 (significant: 0; non-significant: 0; trend: 0) |
Source |
Mapped by significant region |
Gene related studies (count: 0)
Gene related SNPs (count: 0)
Gene related CNVs (count: 0)
Gene related other variant (count: 0)
Gene related regions (count: 1)
Gene related GO terms (count: 17)
Gene related KEGG pathways (count: 2)
ID |
Name |
No. of Genes in ADHDgene |
Brief Description |
hsa04514 |
Cell adhesion molecules (CAMs) |
20 |
Cell adhesion molecules are (glyco)proteins expressed on the......
Cell adhesion molecules are (glyco)proteins expressed on the cell surface and play a critical role in a wide array of biologic processes that include hemostasis, the immune response, inflammation, embryogenesis, and development of neuronal tissue. There are four main groups: the integrin family, the immunoglobulin superfamily, selectins, and cadherins. Membrane proteins that mediate immune cell–cell interactions fall into different categories, namely those involved in antigen recognition, costimulation and cellular adhesion. Furthermore cell-cell adhesions are important for brain morphology and highly coordinated brain functions such as memory and learning. During early development of the nervous system, neurons elongate their axons towards their targets and establish and maintain synapses through formation of cell-cell adhesions. Cell-cell adhesions also underpin axon-axon contacts and link neurons with supporting schwann cells and oligodendrocytes.
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|
hsa05020 |
Prion diseases |
11 |
Prion diseases, also termed transmissible spongiform encepha......
Prion diseases, also termed transmissible spongiform encephalopathies (TSEs), are a group of fatal neurodegenerative diseases that affect humans and a number of other animal species. The etiology of these diseases is thought to be associated with the conversion of a normal protein, PrPC, into an infectious, pathogenic form, PrPSc. The conversion is induced by prion infections (for example, variant Creutzfeldt-Jakob disease (vCJD), iatrogenic CJD, Kuru), mutations (familial CJD, Gerstmann-Straussler-Scheinker syndrome, fatal familial insomnia (FFI)) or unknown factors (sporadic CJD (sCJD)), and is thought to occur after PrPC has reached the plasma membrane or is re-internalized for degradation. The PrPSc form shows greater protease resistance than PrPC and accumulates in affected individuals, often in the form of extracellular plaques. Pathways that may lead to neuronal death comprise oxidative stress, regulated activation of complement, ubiquitin-proteasome and endosomal-lysosomal systems, synaptic alterations and dendritic atrophy, corticosteroid response, and endoplasmic reticulum stress. In addition, the conformational transition could lead to the lost of a beneficial activity of the natively folded protein, PrPC.
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|
Genes shared at least 5 GO terms with NCAM1 (count: 9)
Genes shared at least 2 KEGG pathways with NCAM1 (count: 0)
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